Abstract

Tetanus is an acute, often fatal, neurological disease that is characterised by increased muscle tone and spasms caused by tetanospasmin, which is a protein toxin elaborated by Clostridium tetani; this is an obligate anaerobic, motile Gram-positive rod found in the soil, in animal and occasionally in human faeces, and in house dust, hospitals, and operating theatres.1–3 The incubation period is about seven days and the mortality is high.1 Spores may survive for years and are resistant to various disinfectants and to boiling for 20 minutes.1 Muscles of the jaw, face, and head are involved first because the toxin has to travel along shorter axonal pathways.2 Infection is independent of the size of the wound provided that the blood supply and the oxygenation are compromised.2 Clinical tetanus comprises four symptomatic types: generalised, local, cephalic, and neonatal.2,4,5 Local tetanus is uncommon with a reasonable prognosis.3 Cephalic tetanus is a rare variant of local tetanus that involves 1–3% of all reported cases and several cranial nerves are involved.5 It may follow an injury such as laceration, abrasion, or puncture wound.1 It may be associated with a head injury or middle ear infection. It may follow traditional practices like ear piercing, circumcision, and tattooing, or the mouth may be the point of entry.6 Two-thirds of cases of cephalic tetanus progress to generalised disease that can involve the limb muscles and trunk progressively.3,7 The commonest presenting symptom is trismus. Other manifestations include dysfunction of one or more cranial nerves (often the seventh nerve), facial pain, dysphagia, dysarthria, risus sardonicus (spasms of the face and jaw), stiffness of the neck and back (opisthotonos – an arched back with the body resting on the heels and occiput), spasms, voiding difficulties, abdominal pain and gastrointestinal problems, and mental and emotional problems.5,7 Other presenting symptoms may be fever, nystagmus, diplopia, cardiac disorders and malaise.1,2,7 Episodes of hypotension and bradycardia have been attributed to either withdrawal of sympathetic activity or increased parasympathetic activity. Episodes of hypertension and tachycardia have also been recorded and are thought to be the result of sympathetic stimulation. Spasms may be mild, infrequent and brief, or severe, painful, and exhausting. They can cause cyanosis that threatens ventilation, occur repetitively, and may be spontaneous or provoked by even the slightest auditory, visual or emotional stimulation. They may also be protracted, the patient seeming to be in a state of perpetual convulsion. Spasm of the pharyngeal muscles prevents swallowing of saliva that may be aspirated and cause atelectasis and aspiration pneumonia. Laryngeal spasm may lead to sudden death from asphyxia. The diagnosis of tetanus is based entirely on clinical findings.1,2 The activity of creatine phosphokinase (CPK) may be increased in some cases, but it is not pathognomonic.1 It is of interest that C. tetani can be isolated from wounds of patients without tetanus and often cannot be recovered from wounds of those with tetanus.

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